Homozygous clones in the wing disc survive and do not show polarity defects.
sdtEH681 follicle cell clones, induced by driving Scer\FLP1Scer\UAS.cUa under the control of the Scer\GAL4e22c driver, are morphologically indistinguishable from wild type.
sdtEH681 embryos show reduced cuticle production, typically resulting in embryos with fragmented cuticle.
Homozygous eye clones have no obvious effects on photoreceptor cell morphogenesis. No light-induced retinal degeneration is seen.
Epithelial cells of ectodermal origin lose their apicobasal polarity resulting in the loss of epithelial integrity and cell death. Both epidermal and amnioserosa cells of stage 10 lack zonula adherens junctions (ZA) and the number of spot adherens junctions (SAJ) is lower. The structure of all ectodermally derived epithelia is affected to varying extents.
First defects in zonula adherens formation are seen at the onset of germband extension on the dorsal side of the embryo in the developing amnioserosa. The distribution of adherens junction material at the apicolateral boundary is more irregular.
Cell death is dramatically increased. Although no extra mesoderm cells are induced to become hemocytes the macrophages become larger than average. Cellular debris becomes located extracellularly in the hemolymph.
At stage 11 of embryogenesis ectodermal cells lose their normal columnar shape and round up. 1-2hr later cells form clusters, rather than a monolayer. Dead cells are often seen on the outside of the embryo. Vesicles form of cells retaining epithelial characteristics, and later secrete grains or vesicles of cuticle. Many cells fail to become integrated into an epithelial sheet. Degeneration is most extreme in the epidermis, the pharynx and the amnioserosa, and least extreme in the proventriculus and Malpighian tubules which develop almost normally.
Aberrant organogenesis and small shreds of cuticle.